Brain Track 3 Drugs Flashcards

Question 1

Q

Amphetamine

Answer

A

CLASS: Stimulant MECHANISM: Stimulate release of dopamine and norepinephrine. Smoked or IV can produce abuse and dependence similar to cocaine. High is less intense if taken orally. INDICATION: ADHD and narcolepsy AEs:

Question 2

Q

Anandamide

Answer

A

CLASS: Endogenous cannabinoid MECHANISM: Endogenous ligand for marijuana's receptor. Contains many pharmacologically active compounds, d-9-THC, believed to be responsible for much of effect. G-protein coupled receptor at high density in cerebral cortex, hippocampus, striatum, cerebellum. Found on GABA-mediated inhibitory neurons >> binding decreases GABA release. High includes giddiness, hunger, impaired coordination, cognitive function, learning, memory. Effects last a few hours, rapid tolerance after a few doses. INDICATION: endogenous AEs: endogenous

Question 3

Q

Buprenorphine

Answer

A

CLASS: Opioid partial agonist MECHANISM: Methadone alternative, partial m-agonist, limited efficacy as analgesic. Very tight binding at receptor (moreso than any other opioids or antagonists). Reduced high when taken by addict (like methadone), but can't be given to addict chronically using large doses of opioids >> withdrawal (cf. methadone = no withddrawal symptoms). Decreases drug-seeking & craving (like naltrexone) by preventing pharmacological effect. Sublingual form as individual drug or in combination with naloxone (opioid antagonist >> "Suboxone", used to discourage parenteral administration if extracted from tablet). INDICATION: Opioid substitution therapy (prescribed by PCP's that have taken 8-hour training, to a max of 30 patients in one practice) = more access. Schedule III drug (cf. methadone). AEs: Extremely difficult to displace (even with large doses of full aognists) >> acute painful injury difficult to manage (opioids ineffective for pain, must use non-opioid management, e.g. nerve block, epidural). Must stop therapy days prior to scheduled surgery and prevent withdrawal with short-acting opioids. Can precipitate withdrawal syndrome if given to chronic high-dose opioid user. More expensive cf. methadone.

Question 4

Q

Bupropion

Answer

A

CLASS: Atypical Antidepressant MECHANISM: Diminishes nicotine withdrawal syndrome, less effective at maintaining long-term abstinence cf. varenicline. INDICATION: Nicotine withdrawal prevention AEs:

Question 5

Q

Clonidine

Answer

A

CLASS: a2-agonist MECHANISM: Centrally acting a2-agonist, used to mitigate autonomic symptoms of opioid withdrawal during inpatient detoxification treatment. INDICATION: Detoxification adjuvant AEs:

Question 6

Q

Cocaine

Answer

A

CLASS: Monoamine reuptake inhibitor MECHANISM: Inhibits reuptake of dopamine, norepinephrine, and serotonin. Available as hydrochloride salt (white powder) that is inhaled or injected and as alkaloid base ("crack") that is smoked. Causes euphoria, increased arousal, alertness, concentration. Effects last

Question 7

Q

Disulfiram

Answer

A

<p class="large" style="text-align: center;">CLASS: Aldehyde dehydrogenase inhibitor MECHANISM: Irreversible (lasts about 2 weeks following administration) inhibitor of aldehyde dehydrogenase.  Ingestion of ethanol will lead to unpleasant illness from toxic effect of acetaldehyde accumulation (concentration may increase 10x): face becomes hot, flushed, red, vasodilation spreads throughout body, throbbing headache, nausea, vomiting, (orthostatic) hypotension (potentially dangerous). INDICATION: Long-term management of ethanol abuse. AEs: Consumption of even small amount of alcohol can make patient sick and possibly critically ill.  Must avoid alcohol in sauces, cough syrup, mouthwash, topical aftershave.
2E1 inhibitor (ethanol microsomal oxidation enzyme) and blocks acetaminophen metabolism.</p>

Question 8

Q

Ethanol

Answer

A

CLASS: CNS depressant MECHANISM: Cross-tolerance (one substance can substitute for another to prevent withdrawal, e.g. heavy alcohol user will require more benzos for sedation) with other CNS depressants. Tolerance allows large doses without sedation (different rate of tolerance to sedation cf. apnea = decreases therapeutic index). Detoxification achieved in days (cf. long-acting barbiturate, may take months). May substitute a benzo with longer t1/2 (e.g. oxazepam) with a tapered dose during detoxification period. INDICATION: Substance of Abuse AEs: Withdrawal: status epilepticus, may be fatal. Likelihood of fatal withdrawal based on higher use for longer period. Also, craving, irritability, insomnia, tachycardia, hypertension, hallucinations.

Question 9

Q

Heroin

Answer

A

CLASS: Opioid MECHANISM: Diacetyl derivative of morphine, more lipophilic = faster onset post-IV or inhalation cf. morphine. Intense euphoria (minutes) followed by sedation (hours). Drug abusers will administer 2-4x daily usually. Readily produces tolerance (100-1,000x without causing apnea), withdrawal symptoms appear shortly after last dose of a short-acting opioid. Most abusers don't begin abuse following pain management, and those prescribed for chronic pain that develop tolerance don't usually become addicted. INDICATION: Schedule I Drug (no medical use) AEs: Withdrawal: unpleasant, not life-threatening. Includes craving, hyperalgesia, nausea, abdominal cramps, insomnia, anxiety. Associated signs: mydriasis, fever, sweating, piloerection, vomiting, diarrhea, hypertension, yawning.
Accidental overdose: causes apnea due to variable purity of the drug.

Question 10

Q

Ketamine

Answer

A

CLASS: Psychedelic MECHANISM: Causes hallucinogenic effect. NMDA antagonist. INDICATION: Dissociative anesthetic AEs:

Question 11

Q

Lysergic Acid Diethylamide

Answer

A

CLASS: Psychedelic MECHANISM: Causes hallucinogenic effect, ergot derivative. Hallucinogenic effects primarily from 5-HT2 agonism (cf. newer atypical antipsychotics = 5-HT2 antagonists). INDICATION: Substance of Abuse AEs: Mood changes: euphoria or depression. Altered color and shape perception. "Bad trip" = intense anxiety and dysphoria. Psychedleic and psychotic effects can rarely last for a few days. Tolerance is clinically irrelevent (most don't use this often, repeatedly per day). No withdrawal syndrome. Reported hallucination flashbacks long after last usage (?permanent drug-induced changes to visual cortex).

Question 12

Q

Marijuana

Answer

A

CLASS: Cannabinoid MECHANISM: Contains many pharmacologically active compounds, d-9-THC, believed to be responsible for much of effect. G-protein coupled receptor at high density in cerebral cortex, hippocampus, striatum, cerebellum. Found on GABA-mediated inhibitory neurons >> binding decreases GABA release. High includes giddiness, hunger, impaired coordination, cognitive function, learning, memory. Effects last a few hours, rapid tolerance after a few doses. INDICATION: Most commonly used illegal substance in US. AEs: Withdrawal: mild insomnia, restlessness, irritability, nausea. Main danger from impaired driving.

Question 13

Q

Methadone

Answer

A

CLASS: Opioid MECHANISM: Synthetic opioid, slower onset/offset cf. other opioids = less highs and lows between doses. Daily administration to prevent withdrawal. Tolerance to sedative effects, users on maintenance program are surprisingly functional. Goal is to taper very slowly to prevent withdrawal. INDICATION: Opioid substitution therapy prescribed for withdrawal prevention only by specially licensed clinics (must go every day to get single dose), can be prescribed for analgesia by PCP's. Schedule II drug (cf. buprenorphine) = less access. AEs:

Question 14

Q

Methamphetamine

Answer

A

CLASS: CNS stimulant MECHANISM: Stimulate release of dopamine and norepinephrine. Smoked or IV can produce abuse and dependence similar to cocaine. High is less intense if taken orally. INDICATION: Substance of Abuse AEs: Same as Amphetamine

Question 15

Q

Methylphenidate

Answer

A

CLASS: CNS stimulant MECHANISM: Stimulate release of dopamine and norepinephrine. Smoked or IV can produce abuse and dependence similar to cocaine. High is less intense if taken orally. INDICATION: ADHD and narcolepsy AEs:

Question 16

Q

Naltrexone

Answer

A

CLASS: Opioid antagonist MECHANISM: Following withdrawal syndrome in detoxification program, used for supportive therapy to prevent future opioid abuse. Opioid antagonist used chronically, oral bioavailability. Prevents drug-seeking by blocking effects of opioids (i.e. no point in robbing homes to buy drugs if the drug won't be effective). Also decreases / eliminates craving for opioids in recovering addicts. 1x monthly injection available (alcohol sobriety).
Also, blocks dopaminergic reward pathway in alcohol use. Oral and injection use can decrease heavy-drinking days in alcoholics (modest abstinence efficacy) >> injection is very expensive. INDICATION: Opioid & alcohol sobriety maintenance AEs: Injection is very expensive.

Question 17

Q

Nicotine

Answer

A

CLASS: CNS stimulant MECHANISM: More people dependent on this substance than any other in US. Ganglionic agonist & CNS stimulant with intense reinforcing characteristics. Tolerance develops to effects. Administration by various routes can prevent withdrawal without producing peak levels leading to reinforcement >> gradually tapering dose is successful for eliminating dependence. INDICATION: Substitution therapy for nicotine addiction (gum, lozenge, patch, nasal spray, inhaler) AEs: Majority of smokers wish to quit, but minority attempt quitting, only 5% able to quit without psychotherapeutic or pharmacologic assistance. Withdrawal: insomnia, irritability, anxiety, dysphoria, increased appetite (>> weight gain).

Question 18

Q

Octreotide

Answer

A

CLASS: Somatostatin analogue MECHANISM: Somatostain analogue, used to mitigate gastrointestinal symptoms of opioid withdrawal during inpatient detoxification treatment. INDICATION: Detoxification adjuvant AEs:

Question 19

Q

Phencyclidine

Answer

A

CLASS: Psychedelic MECHANISM: Causes hallucinogenic effect. NMDA antagonist. INDICATION: Veterinary anesthetic AEs: Emotional withdrawal, bizarre response to environmental stimuli. Coma at high dose (preserved ventilation) = desirbale features of anesthetic agent. Prolonged recovery period with hallucinations and delirium.

Question 20

Q

Varenicline

Answer

A

CLASS: Partial nicotinic agonist MECHANISM: "Chantix", Partial agonist at nicotinic (a4b2 subset, ?coupled with dopamine release that stimulates reward pathway) receptor, minimizes withdrawal symptoms without producing peak nicotine lvels associated with reinforcement. INDICATION: Nicotine substitution therapy (24-week regimen) >> 45% abstinent @ 24-weeks, 28% abstinent @ 1 year (modest cf. placebo), but more efficacious than nicotine replacement for maintaining long-term abstinence. AEs: More weight gain cf. nicotine therapy or bupropion.

Question 21

Q

Acamprosate

Answer

A

CLASS: NMDA modulator MECHANISM: Unclear mechanism at NMDA receptor decreases alcohol craving. Efficacy appears higher when used in combination with naltrexone. Effects may last many months following one-year treatment. Studies required participation in behavioral therapy and AA attendance >> otherwise unable to demonstrate therapeutic effect. INDICATION: Alcohol dependence therapy AEs:

Question 22

Q

Dextroamphetamine

Answer

A

CLASS: CNS stimulant MECHANISM: Stimulate release of dopamine and norepinephrine. Smoked or IV can produce abuse and dependence similar to cocaine. High is less intense if taken orally. INDICATION: Substance of Abuse AEs: Same as Amphetamine

Question 23

Q

Dronabinol

Answer

A

CLASS: Cannabinoid derivative MECHANISM: Table form of d-9-THC. G-protein coupled receptor at high density in cerebral cortex, hippocampus, striatum, cerebellum. Found on GABA-mediated inhibitory neurons >> binding decreases GABA release. High includes giddiness, hunger, impaired coordination, cognitive function, learning, memory. Effects last a few hours, rapid tolerance after a few doses. INDICATION: Severe nausea and vomiting associated with chemotherapy. AEs:

Question 24

Q

Gasoline

Answer

A

CLASS: Organic solvent MECHANISM: Abused by children and those without access to other abusable substances, usually via inhalation. Contains medium-length alkanes. Inhalation of vapors causes dizziness and intoxicated feeling. INDICATION: Combustion engine AEs: Short-term: cardiac arrhythmias (hydrocarbons increase automaticity of cardiac cells). Long-term: potentially irreversible brain damage, peripheral nerv, liver, and kidney damage.

Question 25

Q

Mescaline

Answer

A

CLASS: Psychedelic MECHANISM: Causes hallucinogenic effect, peyote derivative. Hallucinogenic effects primarily from 5-HT2 agonism (cf. newer atypical antipsychotics = 5-HT2 antagonists). Effects within 1 hour, last up to 8 hours. INDICATION: Substance of Abuse AEs: Mood changes: euphoria or depression. Altered color and shape perception. "Bad trip" = intense anxiety and dysphoria. Psychedleic and psychotic effects can rarely last for a few days. Tolerance is clinically irrelevent (most don't use this often, repeatedly per day). No withdrawal syndrome. Reported hallucination flashbacks long after last usage (?permanent drug-induced changes to visual cortex).

Question 26

Q

Methaqualone

Answer

A

CLASS: CNS depressant MECHANISM: Cross-tolerance (one substance can substitute for another to prevent withdrawal, e.g. heavy alcohol user will require more benzos for sedation) with other CNS depressants. Tolerance allows large doses without sedation (different rate of tolerance to sedation cf. apnea = decreases therapeutic index). INDICATION: Obsolete nighttime sedative AEs: Withdrawal: status epilepticus, may be fatal. Likelihood of fatal withdrawal based on higher use for longer period. Also, craving, irritability, insomnia, tachycardia, hypertension, hallucinations.

Question 27

Q

Methylenedioxymethamphetamine (MDMA)

Answer

A

CLASS: CNS stimulant & Psychedelic MECHANISM: Hallucinations & Stimulate release of dopamine and norepinephrine. Smoked or IV can produce abuse and dependence similar to cocaine. High is less intense if taken orally. INDICATION: No medical use, "club drug" (user can stay awake and dance for prolonged period) AEs:

Question 28

Q

Psilocybin

Answer

A

CLASS: Psychedelic MECHANISM: Causes hallucinogenic effect, mushroom derivative. Hallucinogenic effects primarily from 5-HT2 agonism (cf. newer atypical antipsychotics = 5-HT2 antagonists). INDICATION: Substance of Abuse AEs: Mood changes: euphoria or depression. Altered color and shape perception. "Bad trip" = intense anxiety and dysphoria. Psychedleic and psychotic effects can rarely last for a few days. Tolerance is clinically irrelevent (most don't use this often, repeatedly per day). No withdrawal syndrome. Reported hallucination flashbacks long after last usage (?permanent drug-induced changes to visual cortex).

Question 29

Q

Toluene

Answer

A

CLASS: Organic solvent MECHANISM: Abused by children and those without access to other abusable substances, usually via inhalation. Major volatile component of model airplane glue. Inhalation of vapors causes dizziness and intoxicated feeling. INDICATION: Model airplane glue AEs: Short-term: cardiac arrhythmias (hydrocarbons increase automaticity of cardiac cells). Long-term: potentially irreversible brain damage, peripheral nerv, liver, and kidney damage.

Question 30

Q

Amphetamine

Answer

A

CLASS: Stimulant MECHANISM: Indirect sympathomimetic, well-absorbed orally, peak effect in 3 hours, t1/2 depends on urinary pH (3-24 hours), metabolized to many products including benzoic acid, stimulates release NE, DA (at low dose), 5-HT (at high dose, seen in abuse) from presynaptic nerve terminal vesicle storage. Dirty CNS drug (a1, a2, b1, b2 activation) = effects often difficult to predict or overwhelmed by peripheral actions (e.g. central a2 agonism contrasts with peripheral a1 agonism). Chiral molecule, racemic mixture of D- and L-isomers no longer available alone. Peripheral effects dose-dependent, b-adrenoceptors (low dose, though clinical doses also activate a-receptors) = tachycardia (b1) and hypertension (b1 inotropy and a1 vasoconstriction). Increased alertness and wakefulness (10-20x caffeine), increased concentration and mood, motor and speech. Delays fatigue onset, need for sleep postponed (though not indefinitely) >> may sleep for prolonged period after effects wane, can have disordered sleep for months following chronic use. Increased ventilatory drive (via medulla action). Appetite suppression (?a1 action in hypothalamic feeding center), with tolerance developing in a few weeks = weight loss not sustained long term. Attention effects at lower doses than needed for prolonged wakefulness, selective activity on neurons projecting to behavior & cognitive brain regions: prefrontal cortex, low dose increases catecholamine release from hippocampal neurons projecting to PFC, decreasing catecholamine release from neurons arising elsewhere (increased "signal-to-noise ratio"). INDICATION: ADHD, Appetite suppression (formerly FDA approved, now sanctionable offense) AEs: Etensions of pharmacologic effect: restlessness, insomnia, talkativenss, irritability. High doses = anxiety, aggressiveness, tremor, hyperactive reflexes, fever, sweating, dry mouth, nvd, abdominal cramping. Larger doses (increased serotonin release) = delirium, hallucination, paranoia, panic, suicidality, homicidality; more likely if underlying mental illness (or anyone in large enough dose).
Cardiovascular: hypertension, tachycardia; higher dose = HA, arrhythmia, palpitations, angina, hypotension circulatory collapse.
Fatal: seizure, intracranial hemorrhage (seen at autopsy).
Overdose treatment: induce vomiting, activated charcoal, gastric lavage, decrease urinary pH (increase excretion rate), a- or b-antagonists (symptomatic treatment), benzos (decrease CNS activity).
Long-term treatment: decreased growth rate in children (if administered continuously without holiday to allow rebound growth), sudden cardiac death (very rare, increased if preexistent structural or conduction abnormalities = screening ECG and echo before starting therapy), hypertension (elevated if preexisting hypertension, may need to modify Rx regimen), mania (if bipolar & ADHD, stimulants may increase manic episodes), psychosis (if predisposed, may unmask with stimulants). No reported increase in suicidal ideation or action at recommended dose. Schedule II drug.

Question 31

Q

Atomoxetine

Answer

A

CLASS: SNRI MECHANISM: Not a stimulant, selective NE reuptake inhibitor (not tricyclic antidepressant). INDICATION: ADHD AEs: Black Box: increased suicidal ideation risk in adolescents (like other antidepressant), despite surveillance demonstrating lack of increased suicide incidence.
Early therapy: fatigue and somnolence (cf. stimulants), typically develop tolerance to these effects within a few weeks. Anorexia, abdominal pain.

Question 32

Q

Methamphetamine

Answer

A

CLASS: Stimulant MECHANISM: Same action as amphetamine: neurotransmitter release, additionally decreases NT reuptake (especially doopamine). Greater CNS selectivity cf. amphetamine = more likely abused and dependence. Additionally, nonselective MAOI. Mostly synthesized in illegal labs (for abuse) using pseudoephedrine OTC + hydroiodic acid >> iodoephedrine, reduced by red phosphorus. INDICATION: ADHD AEs: High dose chronic use = dopaminergic neuron damage & psychosis / Parkinson Disease. Cardiomyopathy, "meth mouth" (premature loss of teeth from poor oral hygiene + xerostomia). Most highly addictive stimulant.
Withdrawal: not life-threatening, but protracted with depression, hypersomnia, anhedonia, psychosis (that may be permanent).

Question 33

Q

Methylphenidate

Answer

A

CLASS: Stimulant MECHANISM: "Ritalin", contains structure of methamphetamine and shared mechanism. Greater lipid solubility cf. amphetamine and methamphetamine = greater ratio of CNS:peripheral effects. Marketed as racemic mixture, D-isomer more potent. Tolerance tends not to develop at low (clinical) dose = dose escalation not necessary (except with growing child). Drug holidays often prescribed in long-term therapy = withdrawal uncommon. INDICATION: ADHD, narcolepsy, increased energy in elderly (off-label). AEs: Long-term treatment: decreased growth rate in children (if administered continuously without holiday to allow rebound growth), sudden cardiac death (very rare, increased if preexistent structural or conduction abnormalities = screening ECG and echo before starting therapy), hypertension (elevated if preexisting hypertension, may need to modify Rx regimen), mania (if bipolar & ADHD, stimulants may increase manic episodes), psychosis (if predisposed, may unmask with stimulants). No reported increase in suicidal ideation or action at recommended dose. Schedule II drug.

Question 34

Q

Modafinil

Answer

A

CLASS: Stimulant MECHANISM: Unknown mechanism, increases wakefulness. Racemic mixture, not amphetamine = no cardiovascular effects, sleep effects. Euphoria and reinforcing behavior, but considered low abuse potential (Schedule IV drug). INDICATION: Narcolepsy, daytime somnolence from OSA, shift work sleep disorder, jet lag (off-label). AEs: Minimal, rare Stevens-Johnson syndrome

Question 35

Q

Aromodafinil

Answer

A

CLASS: Stimulant MECHANISM: R-isomer of modafinil, new preparation. INDICATION: see modafinil AEs: see modafinil

Question 36

Q

Dextroamphetamine

Answer

A

CLASS: Stimulant MECHANISM: D-isomer of amphetamine. 4x (relatively low potency ratio cf. opioids: may have 10,000x difference between enantiomers) potency cf. L-amphetamine in increasing neurotransmitter release. Combination with racemic mixturein 3:1 D- to L-isomer mass ratio = "Adderall". Immediate-release tablets, sustained-release capsules (contains some particles immediately absorbed and some with delayed absorption) available. INDICATION: Narcolepsy, ADHD (sustained release 1x daily) AEs:

Question 37

Q

Aspirin

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: COX-inhibitor prototype, COX-1 selective via covalent reaction (acetylation) with permanent enzyme inhibition. Resolution of effect requires synthesis of new COX (happens rapidly), but essentially kills platelets (because they can't carry out protein synthesis).
Biphasic dose-response: Post-MI 81 mg dose recommended, b/c 100% liver metabolism = ~0 circulating ASA (only results in platelet inhibition as circulate through liver, without systemic PGI2/anticoagulant inhibition). Low dose = anticoagulant, High dose = diminished anticoagulant effect. INDICATION: WHO Step 1 (1-3 Scale) pain, Analgesia, antiinflammatory, antipyresis (similar duration cf. ibuprofen) >> Anti-platelet (increased BT lasts ~1 week). Post-MI AEs: Rapid: heartburn, nausea, vomiting (from central and peripheral actions)
Later: ulcer, bleeding (painless), melena, hematemesis
High dose: tinnitus (reversible), acute renal failure (in patients that depend on PG for perfusion), HSR (increased risk if asthma and nasal polyps)

Question 38

Q

Acetaminophen

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: 50% inhibition of COX-1 and COX-2 with no antiinflammatory activity. INDICATION: WHO Step 1 (1-3 Scale) pain, Similar analgesia and antipyresis cf. ASA, only COX-inhibitor to use in 3rd trimester (won't close ductus arteriosus). Can increase analgesia with co-administration with COX-inhibitor. AEs: No COX-related AE's (platelets, GI, renal), no HSR for patients with Hx of COX-inhibitor drug reaction.
Fatal hepatic necrosis with significant overdose (important to include doses from combination medications in total daily intake)

Question 39

Q

Ibuprofen

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: Older, non-selective, reversible COX-inhibitor. Brief platelet inhibition, OTC and Rx available (same formula). Analgesia and antipyresis via PG synthesis blockade. COX-1 PG's = TXA2 synth/platelet adhesion, GI integrity, GFR, nociception; COX-2 PG's = inflammatory response & resolution, GI adaptive cytoprotection, renal Na+ balance, kidney development, angiogenesis, endothelial PGI2 synth, MI damage protection. INDICATION: WHO Step 1 (1-3 Scale) pain, Analgesia, antiinflammatory, antipyresis AEs: GI effects less than ASA

Question 40

Q

Naproxen

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: Like ibuprofen, but longer duration. Taken orally, available OTC. INDICATION: WHO Step 1 (1-3 Scale) pain, Antiinflammatory, analgesic, antipyresis AEs: GI upset

Question 41

Q

Indomethacin

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: Antiinflammatory, decreases PMN motility, decreases mucopolysaccharide synthesis, vasoconstricts. Higher efficacy cf. other COX-inhibitors. INDICATION: WHO Step 1 (1-3 Scale) pain, Antiinflammatory, analgesic, antipyresis AEs: GI upset

Question 42

Q

Ketorolac

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: Effective parenteral opioid alternative, COX-1 selective. Can increase analgesia with minimal toxicity. IM route is slower (peaks at 1 hour), IV route is faster (peaks at 1-2 minutes) >> IM effect is prolonged and allows increased dosing interval. INDICATION: WHO Step 1 (1-3 Scale) pain, First reliable morphine substitute for severe pain. Co-administration with morphine allows 50% reduction in opioid treatment. AEs: Do not use >5 days (25% will get ulcer with 1 week of use). Do not use pre-surgery (platelet inhibition and delayed healing).

Question 43

Q

Celecoxib

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: First selective COX-2 inhibitor (later discovered that diclofenac and etodolac have COX-2 selectivity), lacks ability to inhibit platelet's TXA2 synthesis. Unlike opioids, COX-inhibitors have "ceiling effect" = unable to relieve severe levels of pain by increasing dose. INDICATION: WHO Step 1 (1-3 Scale) pain, Analgesia (within pain ceiling), inflammatory-related pain (antiinflammatory actions make a better choice than opioids), opioid-sparing (titrate to ceiling/maximal tolerable dose, then add opioid if analgesia is inadequate). Can use in combination with APAP to increase ceiling without increasing toxicity. Arthritis (slow GI absorption and onset). AEs: Less AE's than non-selective COX inhibitors

Question 44

Q

Baclofen

Answer

A

CLASS: MECHANISM: GABA-B receptor agonist in spinal cord, increases neuronal inhibition by interneurons. Can improve severe muscle spasticity via central muscle relaxation. INDICATION: WHO Step 1 (1-3 Scale) pain, Trigeminal neuralgia, ALS spasticity AEs:

Question 45

Q

Diclofenac

Answer

A

CLASS: Non-opioid Analgesic MECHANISM: COX inhibitor, topical available.
Phase 1: Competitive, time dependent, reversible COX inhibitor.
Phase 2: with time, conformational change with tighter binding. Class 2 NSAID. INDICATION: WHO Step 1 (1-3 Scale) pain, arthritis AEs: Increase COX-1 selectivity increases risk of ulcer and GI risks.

Question 46

Q

Codeine

Answer

A

CLASS: Opioid Analgesic MECHANISM: Molecule is morphine O-methylated at position 3. Usually given orally, 10% O-demethylated by CYP2D6 to morphine >> accounts for codeine's therapeutic effect. Not effective in 10% caucasians with 2D6 deficiency (though still active antitussive) INDICATION: WHO Step 2 (4-6 Scale) pain, analgesia, antitussive. AEs: Nausea, CNS effects (dysphoria and agitation rarely)

Question 47

Q

Oxycodone

Answer

A

CLASS: Opioid Analgesic MECHANISM: No IV form, oral only, and in combination with acetaminophen ("Percocet" and "Tylox"), similar duration cf. morphine. Long-acting form ("Oxycontin") INDICATION: WHO Step 2 (4-6 Scale) pain, long-acting form for chronic pain. AEs:

Question 48

Q

Morphine

Answer

A

CLASS: Opioid Analgesic MECHANISM: IV or PO, long-acting PO. Opioids act primarily to alter perception of pain as noxious (still perceived as present). T-shaped, 5-ringed molecule, only the optically active, L-form provides analgesia. Relief of pain at doses that don't produce sleep or reduce sensation. Direct inhibition of pain signaling at dorsal horn and rostrad transmission of pain is decreased by activating descending inhibitory pathways from brainstem. Emotional response to pain altered by action on limbic cortex. Relief of pain can lead to sleep, mood elevation, frank euphoria. 30-60 minute peak, 3-4 hour duration. Causes peripheral vasodilation by depressing medullary vasomotor centers. Least lipophilic opioid = slower membrane pentration and less fatty tissue accumulation. Rapid absorption via IV, IM, subQ, oral (30% bioavailable), 25-35% bound to plasma proteins, large Vd, hepatic elimination (rapid, flow-dependent, 70% per pass = short t1/2) transforms to morphine-3/6-glucuronide (active metabolite, may account for long duration of morphine effect) or demethylates to normorphine (can be excreted in urine or bile). Peak analgesia by IV at 30-60 minutes (poor CNS penetration rate). INDICATION: WHO Step 2 (4-6 Scale) pain, any level pain relieved (with sufficient dose), especially effective on chronic pain (less so with sharp, acute pain or neuropathic pain). Cough suppression via actions on medullary cough center (different receptor cf. analgesia/respiratory depression). AEs: High abuse potential. Drowsiness, sense of heaviness, difficulty concentrating. Hypnosis at high dose, but no amnesia at subhypnotic dose (cf. benzodiazepines). CNS effects (dysphoria and agitation rarely), respiratory distress = typical cause of death from overdose (dose-dependent depressed response to CO2/pH, decreased RR not sensitive indicator of opioid effect). Rarely cause respiratory depression at analgesic dose unless preexisting pathology (e.g., hypothyroid, CNS disease) or concurrent drug use (alcohol, general anesthetics, benzodiazepines, barbiturates). Large dose causes inadequate ventilation and Cheyne-Stokes breathing. Equianalgesic doses cause equivalent respiratory depression. Miosis is pathognomonic for opioid overdose. Activates vomiting center in medullary area postrema, especially in ambulatory patients. Bradycardia via central action on vagus nerve. Orthostatic hypotension from vasodilation. IgE-mediated histamine release from mast cells. Can prevent CV effects by H1/H2-blocking (doesn't stop histamine release). Constipation (from anal sphincter spasm and delayed intestinal transit time), biliary colic (via spasm of Sphincter of Oddi and contraction along biliary tree). Neonatal physical dependence and withdrawal (if mother abusing opioids during pregnancy >> can be life threatening) and neonatal respiratory depression (from parenteral opioids used to treat labor pain). Withdrawal syndrome following physical dependence and abrupt removal of drug can be stopped with small doses of IV morphine.
Tolerance: to depressant effects (analgesia, euphoria, and respiratory depression), begins with decreased duration of analgesia following dose, then decreased effect intensity. Can be overcome with higher doses, but some individuals may present with profound tolerance requiring massive doses to elicit effect. Tolerance often does not occur with regard to stimulant (constipation, pupillary constriction) effects.

Question 49

Q

Hydromorphone

Answer

A

CLASS: Opioid Analgesic MECHANISM: "Dilaudid," First semisynthetic opioids, made by simple morphine substitution. 10-20 minute peak, 2-3 hour duration. 7x more potent parenterally cf. morphine without histamine release. Similar duration INDICATION: WHO Step 2 (4-6 Scale) pain, parenteral and oral administration for acute and chronic pain (morphine alternative). AEs: Less histamine release

Question 50

Q

Methadone

Answer

A

CLASS: Opioid Analgesic MECHANISM: Long t1/2 (terminal t1/2 ~35 hours) = repeated doses may accumulate resulting in appearance of longer lasting subsequent doses. 15-30 minute peak, 3-4 hour duration. Long-lasting synthetic opioid, equipotent cf. morphine with high oral bioavailability (80%), more lipid soluble and more protein binding. Very large Vd with low clearance, similar duration cf. morphine following bolus. INDICATION: WHO Step 2 (4-6 Scale) pain AEs:

Question 51

Q

Meperidine

Answer

A

CLASS: Opioid Analgesic MECHANISM: [ARCHAIC DRUG] Made by opening ring between C12 and C13 on morphine. Structurally analogous to tyrosine (which must be in terminal position for peptide opioid activity. 5-7 minute peak, 2-3 hour duration. Weakly atropinic, doesn't cause bradycardia. More lipophilic cf. morphine, faster analgesia with shorter duration. Larger Vd and higher rate of hepatic clearance. More protein bound (65-80%) to a1-acid glcyoprotein. Rapid demethylation to normeperidine (potent convulsive, t1/2 8-12 hours) >> seizures in renal failure. Has serotonin reuptake inhibitory effects. INDICATION: WHO Step 2 (4-6 Scale) pain AEs: Toxic metabolite, normeperidine (Do not use!) = seizures, CNS effects (dysphoria and agitation rarely). IgA-mediated anaphylaxis reported. Fatal interaction with MAOi's (from serotonin reuptake inhibition) >> serotonergic crisis (agitation, hyperreflexia, hyperthermia).

Question 52

Q

Butorphanol

Answer

A

CLASS: Opioid Analgesic MECHANISM: Agonist-antagonist, k-receptor partial agonist = binding affinity but no efficacy at m-receptor >> competitive morphine antagonist. Intranasal spray, by removal of oxygen between C4 and C5 on morphine. 15-30 minute peak, 2-3 hour duration. No abuse potential. INDICATION: WHO Step 2 (4-6 Scale) pain, Acute and chronic pain, for pts with biliary colic post-morphine (no biliary colic sx) AEs: Drowsiness, mood effects (different cf. pure agonists) = "apathetic sedation," floating and dissociative sensation without mood elevation. Appear extremely sedated, yet capable of lucid conversation. Tolerable respiratory depression. Less constipation, urinary retention. Mild opioid withdrawal syndrome.

Question 53

Q

Buprenorphine

Answer

A

CLASS: MECHANISM: Oral, > reduces opioid effect when given following morphine. No abuse potential. INDICATION: Acute and chronic pain, opioid reversal (strong antagonist), for pts with biliary colic post-morphine (no biliary colic sx) AEs: Drowsiness, mood effects (different cf. pure agonists) = "apathetic sedation," floating and dissociative sensation without mood elevation. Appear extremely sedated, yet capable of lucid conversation. Tolerable respiratory depression. Less constipation, urinary retention. Mild opioid withdrawal syndrome.

Question 54

Q

Diphenoxylate

Answer

A

CLASS: MECHANISM: Opioid, used for poor absorption with oral administration = no central effects, acts by inducing constipation. "Lomotil" INDICATION: Treat Diarrhea AEs:

Question 55

Q

Heroin

Answer

A

CLASS: MECHANISM: First semisynthetic opioids, made by simple morphine substitution. INDICATION: AEs:

Question 56

Q

Loperamide

Answer

A

CLASS: MECHANISM: Opioid, used to for poor absorption with oral administration = no central effects, acts by inducing constipation. "Imodium" INDICATION: Treat Diarrhea AEs:

Question 57

Q

Methylnaltrexone

Answer

A

CLASS: MECHANISM: Quaternary naltrexone analogue, without good CNS concentration to block opioid-induced (morphine or methadone) bowel dysfunction. Reverses depressed gastric emptying and intestinal motility without blocking analgesia. subQ every other day. INDICATION: Reverse bowel dysfunction from opioid administration AEs:

Question 58

Q

Nalbuphine

Answer

A

CLASS: MECHANISM: Agonist-antagonist, k-receptor partial agonist = binding affinity but no efficacy at m-receptor >> competitive morphine antagonist. 15-30 minute peak, 3-4 hour duration. No abuse potential. INDICATION: Acute and chronic pain, for pts with biliary colic post-morphine (no biliary colic sx), opioid reversal (strong antagonist). AEs: Drowsiness, mood effects (different cf. pure agonists) = "apathetic sedation," floating and dissociative sensation without mood elevation. Appear extremely sedated, yet capable of lucid conversation. Tolerable respiratory depression. Less constipation, urinary retention. Opioid withdrawal syndrome.

Question 59

Q

Naloxone

Answer

A

CLASS: MECHANISM: Made by replacing the methyl substituent on the piperidine nitrogen of morphine (N-allyl derivative) with a bulkier chemical group, has competitive antagonist activity at all m-receptors. Small doses reverse pure opioid agonists and most mixed agonist-antagonists (reversible: can be overcome with additional agonist). Limited effect in opioid-naive person without pain (mild increase HR, BP, slowed EEG a-wave in large dose). Large Vd, easily crosses BBB, rapid hepatic clearance. Opioid reversal can cause increased BP, HR, plasma catecholamines. INDICATION: Opioid reversal, Rapidly reverses miosis from opioid overdose. AEs: Fulminant pulmonary edema, dysrhythmia, death from opioid reversal effects.

Question 60

Q

Naltrexone

Answer

A

CLASS: MECHANISM: Pure antagonist (cf. naloxone), oral and as microsphere injection of embedded medication. High dose will block euphoric effect of heroin to prevent relapse and decrease drug craving (?sobriety in alcoholics). INDICATION: Treat previously detoxified heroin addicts. AEs:

Question 61

Q

Nalorphine

Answer

A

CLASS: MECHANISM: [No longer used clinically] Made by replacing the methyl substituent on the piperidine nitrogen of morphine (N-allyl derivative) with a bulkier chemical group, has agonist-antagonist activity: Agonist-antagonist, k-receptor partial agonist = binding affinity but no efficacy at m-receptor >> competitive morphine antagonist. morphine antagonist, but nearly equipotent cf. morphine in postoperative pain & can reverse morphine analgesia (dependent on ratio >> low-dose reversal, high-dose agonism). Partial agonist (lower maximal effect cf. morphine = ceiling effect to analgesia and toxicity). Unlikely to be abused, precipitates violent withdrawal in addicts. INDICATION: Acute and chronic pain AEs: Violent withdrawal, respiratory depression, sedation, miosis, severe psychotomimetic reaction (at analgesic dose), dysphoria, hallucination. Drowsiness, mood effects (different cf. pure agonists) = "apathetic sedation," floating and dissociative sensation without mood elevation. Appear extremely sedated, yet capable of lucid conversation.

Question 62

Q

Pentazocine

Answer

A

CLASS: MECHANISM: Oral. Agonist-antagonist, k-receptor partial agonist = binding affinity but no efficacy at m-receptor >> competitive morphine antagonist. Made by opening the C5-8 ring on morphine. 15-30 minute peak, 2-3 hour duration. No abuse potential. INDICATION: Acute and chronic pain, for pts with biliary colic post-morphine (no biliary colic sx) AEs: Drowsiness, mood effects (different cf. pure agonists) = "apathetic sedation," floating and dissociative sensation without mood elevation. Appear extremely sedated, yet capable of lucid conversation. More likely to feel "weird" feelings, dysphoria, hallucinations with increased dose. Less constipation, urinary retention. Opioid withdrawal syndrome.

Question 63

Q

Fentanyl

Answer

A

CLASS: Opioid Analgesic MECHANISM: IV or transdermal (no PO form), closely related to meperidine class. 3-5 minute peak, 0.5-1 hour duration. Extremely fat-soluble = rapid onset and short duration. After IV administration, goes to brain, heart, highly perfused tissues (i.e. "central compartment"). Easily crosses BBB, INDICATION: WHO Step 2 (4-6 Scale) pain, not generally for acute pain AEs:

Question 64

Q

Tramodol

Answer

A

CLASS: Opioid Analgesic MECHANISM: Oral only, Not schedule II, partially adrenergic action, T precipitate withdrawal when given to opioid-dependent individuals. INDICATION: WHO Step 2 (4-6 Scale) pain AEs: Can cause serotonergic crisis (if co-administered with MAOi or other reuptake inhibitors), less ventilatory depression and abuse potential cf. typical m-agonists.

Answer 65

A

CLASS: Adjuvant Analgesic MECHANISM: Antidepressant, blocks 5-HT uptake with limited NE uptake block INDICATION: Used in combination with pain medicine for neuropathic or chronic pain, trigeminal neuralgia AEs: Highly sedating, anticholinergic, moderate orthostatic hypotension, arrhythmogenic

Answer 66

A

CLASS: Adjuvant Analgesic MECHANISM: Antidepressant, strongly blocks 5-HT and NE uptake. INDICATION: One of few antidepressants with FDA indication for pain, trigeminal neuralgia AEs: Low sedation, no anticholinergic effects, no orthostatic hypotension, no arrhythmogenicity

Answer 67

A

CLASS: Adjuvant Analgesic MECHANISM: Anticonvulsant and antiarrhythmic (not approved by FDA for treatment of pain), slows recovery of voltage-gated Na+ channels to stabilizes neuronal membrane INDICATION: Used in combination with pain medicine for neuropathic or chornic pain, e.g. trigeminal neuralgia AEs:

Answer 68

A

CLASS: Adjuvant Analgesic MECHANISM: Anticonvulsant and antiarrhythmic (not approved by FDA for treatment of pain), slows recovery of voltage-gated Na+ channels to stabilizes neuronal membrane INDICATION: Used in combination with pain medicine for neuropathic or chornic pain, e.g. trigeminal neuralgia AEs: Stevens Johnson

Answer 69

A

CLASS: Adjuvant Analgesic MECHANISM: Anticonvulsant and antiarrhythmic (not approved by FDA for treatment of pain), slows recovery of voltage-gated Na+ channels to stabilizes neuronal membrane INDICATION: Used in combination with pain medicine for neuropathic or chornic pain AEs:

Answer 70

A

CLASS: Primary Anxiolytic MECHANISM: Distinct structure, cf. diazepam (4 rings cf. 3 rings). INDICATION: Panic disorder, agoraphobia AEs:

Answer 71

A

CLASS: Primary Anxiolytic MECHANISM: 5-HT1A partial agonist little activity at DA or GABA receptors. Does not cause sedation or have anticonvulsant effect. Tolerance to effects does not develop. No cross-tolerance with other benzos / CNS depressants. Less anxiolysis (cf. diazepam) = not for panic attacks INDICATION: For use in patients at risk for abusing benzodiazepines. AEs:

Answer 72

A

CLASS: Primary Anxiolytic MECHANISM: INDICATION: Anticonvulsant, panic disorders AEs:

Answer 73

A

CLASS: Primary Anxiolytic MECHANISM: "Valium". Potentiates inhibitory neurotransmitter, GABA, by increasing GABA-receptor affinity. Additional mechanism responsible for antianxiety effects (because barbiturates and general anesthetics also have this mechanism without anxiolysis). Binds benzo receptor near GABA-receptor (causes increased chloride conductance = hyperpolarization), decreased excitability antagonizes effect of excitatory neurotransmitters. Mimics endozepines (endogenous benzo ligands) activity. Sedation usually perceived as pleasant (cf. antipsychotics, unpleasant sedation), anterograde amnestic effect (even if don't appear sleepy), lessens anxiety symptoms. Tolerance to sedative (not anxiolytic) effect develops. Rapid oral absorption, 90% plasma protein bound, large Vd, small clearance, t1/2 ~20 hours, metabolized to nordiazepam (active with t1/2 = 100 hours). Not water-soluble, parenteral solution with propylene glycol. Painful IV administration, poorly absorbed IM. INDICATION: Anxiolysis, anticonvulsant, generalized anxiety disorder AEs: Sedation and ataxia. Can cause disinhibition leading to inappropriate behavior, ventilatory depression (but rarely apnea, even in large doses) >> greatly potentiated by other depressants (e.g. alcohol, opioids). Does not suppress REM sleep (cf. barbiturates and alcohol), increases time in Stage 4 sleep and overall sleep time.
Tolerance develops readily, withdrawal syndrome won't appear for several days (due to long-acting metabolite) and may include seizures (safer to gradually taper rather than discontinue abruptly).

Answer 74

A

CLASS: Primary Anxiolytic MECHANISM: Endogenous ligand for benzo receptor, regulates the balance of anxiety and calm. Generally significant baseline effect. INDICATION: AEs:

Answer 75

A

CLASS: Primary Anxiolytic MECHANISM: Inverse agonist at benzodiazepine receptor (combined with diazepam does not equate to complete innocuity) INDICATION: Accidental or intentional benzo overdose (only if unsafe excessive benzo dose taken) AEs: Because of baseline endozepine effect (normal anxiety/calm balance regulation), excessive dose may produce extreme agitation. Repeated dosing necessary (shorter-acting than benzos).

Answer 76

A

CLASS: Primary Anxiolytic MECHANISM: SSRI, no chance of dependency, long-term efficacy (cf. benzos and buspirone). INDICATION: OCD, panic attack, PTSD, PMDD, SAD, bulimia AEs:

Answer 77

A

CLASS: Primary Anxiolytic MECHANISM: Benzodiazepine, longer duration of action cf. diazepam. INDICATION: AEs:

Answer 78

A

CLASS: Primary Anxiolytic MECHANISM: Benzodiazepine, active metabolite of diazepam converted to inactive glucuronide = shorter duration. INDICATION: Nighttime sedative (no hangover) AEs:

Answer 79

A

CLASS: Primary Anxiolytic MECHANISM: SSRI, no chance of dependency, long-term efficacy (cf. benzos and buspirone). INDICATION: OCD, panic attack, PTSD, PMDD, SAD, bulimia AEs:

Answer 80

A

CLASS: Primary Anxiolytic MECHANISM: SSRI, no chance of dependency, long-term efficacy (cf. benzos and buspirone). INDICATION: OCD, panic attack, PTSD, PMDD, SAD, bulimia AEs:

Answer 81

A

CLASS: Secondary Anxiolytic MECHANISM: Benzodiazepine, converted to diazepam. INDICATION: AEs:

Answer 82

A

CLASS: Secondary Anxiolytic MECHANISM: SSRI, no chance of dependency, long-term efficacy (cf. benzos and buspirone). INDICATION: OCD, panic attack, PTSD, PMDD, SAD, bulimia AEs:

Answer 83

A

CLASS: NK1 Antagonist MECHANISM: NK1 antagonist (substance P receptor), few AE's or DDI's. INDICATION: Antiemetic for anesthesia (give prior to induction) AEs:

Answer 84

A

CLASS: Dopamine antagonist MECHANISM: DA antagonist, similar to haloperidol, antiemetic dose below that of sedation. INDICATION: Antiemetic for anesthesia (give prior to induction) AEs: Higher doses: excess sedation (unpleasant), extrapyramidal effects (rigidity, dystonia, akathisia).

Answer 85

A

CLASS: IV Anesthetic MECHANISM: Minimal CV effects (following usual induction dose, no change in HR, BP, CO, SVR) is unique among all anesthetics. INDICATION: AEs: High incidence of postoperative nausea and vomiting cf. all other agents. Pain on injection, involuntary movement, hiccough. Inhibits CYP11B = cortisol synthesis, clinical significance of this is unclear.

Answer 86

A

CLASS: Opioid MECHANISM: High lipid solubility, more rapid action onset (3-5 minute peak effect), shorter duration of action from redistribution out of central compartment. No histamine release (cf. morphine), given by intermittent bolus injection (with subsequent doses lasting longer due to redistribution). INDICATION: Analgesia during anesthesia AEs: Skeletal muscle rigidity (especially in large dose by rapid IV injection) >> seen in chest wall, head, and neck muscles, may lead to inability to ventilate (reverse with polarizing/non-depolarizing muscle relaxants).

Answer 87

A

CLASS: Inhalation Anesthetic MECHANISM: Most soluble volatile agent, highest MAC (alveolar concentration of gas at which 50% of individuals do not move in response to skin incision), slowest inhaled wash-in/wash-out speed. Sweet odor, non-irritating to respiratory tree. Excellent skeletal muscle relaxation, splanchnic perfusion decreased. INDICATION: [No longer used in US] AEs: Decreased ventilatory drive, dose-dependent hypotension (from decreased CO). Junctional/nodal cardiac rhythm, increases sensitivity to catecholamine-induced ventricular arrhythmias. Cerebrovascular vasodilation and increased intracranial pressure.
Severe AE's: rare, fatal hepatic necrosis (RF's = obesity, repeated halothane exposure). Malignant hyperthermia (in genetically susceptible patient).

Answer 88

A

CLASS: Inhalation anesthetic MECHANISM: Most common volatile anesthetic, halogenated ether, MAC ~1.2%, pungent odor, may burn on inhalation, decreases ventilatory drive, dilates bronchial smooth muscle. Skeletal muscle relaxation and decreased splanchnic perfusion less cf. halothane. 99.9% expired unchanged. INDICATION: AEs: Hypotension (from decreased SVR) with little effect on CO. Increased HR, but arrhythmias uncommon (cf. halothane).

Answer 89

A

CLASS: IM Anesthetic MECHANISM: Only IM agent available, NMDA receptor antagonist, anesthetic state known as dissociative anesthesia (not like normal sleep, patient appears dissociated from environment, may vocalize, open eyes, track with eyes), but no response to noxious stimuli or event recall. Profound analgesia, persists into postoperative period, vivid dreams, hallucinations (may be perceived as unpleasant). Increases cerebral blood flow and ICP. CV stimulation (increased HR, BP, CO), minimal ventilatory depression (may not ablate airway reflex), significant bronchodilation. Long duration cf. other induction agents, usual IV dose lasts 10-15 minutes = longer recovery. INDICATION: IM induction agent, or in hemodynamic compromise (e.g. CHF) AEs: Contraindicated in intracranial pathology (increased ICP), unpleasant emergence (mitigated by concurrent administration of benzodiazepine or propofol).

Answer 90

A

CLASS: Benzodiazepine MECHANISM: Benzodiazepine INDICATION: Premedicant for anesthesia: sedation, amnesia, and anxiolysis AEs: May prolong recovery.

Answer 91

A

CLASS: Inhalation Anesthetic MECHANISM: Inhalation Anesthetic, fastest inhaled wash-in/wash-out speed. Only inhaled anesthetic that is gas at room temperature, least soluble inhaled anesthetic, MAC is 110% (not obtainable at atmospheric P), give at 50-75% in O2 with concurrent volatile or IV anesthetics for adequate anesthesia. Colorless, odorless, tasteless = well-tolerated, minimal non-CNS effects (little HR, BP, CO, ventilatory drive changes or muscle relaxation). Eliminated by exhalation. Does not trigger malignant hyperthermia. INDICATION: AEs: Higher risk of postoperative nausea and vomiting. Problems if patient has gas contained in closed space (e.g. bowel obstruction, pneumothorax), can diffuse into space and increase volume

Answer 92

A

CLASS: Serotonin Antagonist MECHANISM: Selective 5-HT3 anatagonist, few AE's or DDI's. INDICATION: Antiemetic for anesthesia (give prior to induction) AEs:

Answer 93

A

CLASS: IV Anesthetic MECHANISM: Most common IV anesthetic, for induction rapidly and well-tolerated. Sleep within one arm-to-brain circulation time (15-30 seconds), rapid recovery with few postoperative effects. Insoluble in water, emulsion of oil, glycerol, lecithin. Profound CNS depression: brain metabolic activity (O2 consumption) and EEG are depressed. Decreased cerebral blood flow and ICP. Potentiates action of GABA at GABAa-receptor. Dilates capacitance vessels, decreases cardiac contractility = hypotension, decreased CO; effects exaggerated in hypovolemia and CHF. Inhibits baroreceptor reflex (no significant reflex increase in HR to hypotension). Drug concentration following injection drops rapidly from redistribution (tissue outside central compartment). Accumulates in peripheral tissue = effect duration increases with subsequent dose. INDICATION: IV induction (superior recovery, shorter psychomotor impairment, greater sense of well-being from euphoric effect) AEs: Ventilatory depression (often apnea, with reduced hypercarbic/hypoxic ventilatory response post-awakening). Pain on injection, minimized in larger vein or slower infusion, but not a tissue irritant. Low incidence of post-operative nausea/vomiting (antiemetic properties).

Answer 94

A

CLASS: Opioid MECHANISM: Newest opioid, ester rapidly metabolized by tissue esterases = give as loading dose, then continuous infusion. Patients emerge rapidly (independent of duration of infusion). Dose does not need to adjust for age, weight, gender, hepatic or renal failure. Equipotent cf. fentanyl. INDICATION: Analgesia during anesthesia where rapid emergence desirable (not if expect substantial postoperative pain >> choose alternative analgesic) AEs:

Answer 95

A

CLASS: Muscarinic antagonist MECHANISM: Muscarinic cholinergic antagonist, transdermal patch effective at 4-6 hours, lasts for 3 days = placement night before surgery. INDICATION: Antiemetic for anesthesia (give prior to induction) AEs: Dry mouth, blurred vision (common). Contraindicated in glaucoma and bladder outlet obstruction. Loading dose in adhesive >> must wash hands after handling patch (avoid eye contact).

Answer 96

A

CLASS: Barbiturate MECHANISM: Highly alkaline, irritating if extravasates. CV effects similar to propofol, except no block of baroreceptor reflex (e.g. hypotension induces tachycardia). Pentobarbital is active metabolite. INDICATION: IV induction [No longer available in US] AEs: Hyperalgesia in subanesthetic doses. Hangover (drowsiness, lack of concentration, nausea) lasts longer cf. propofol. Acute illness or death in patients with porphyrias (from heme synthesis enzyme induction) from elevated d-ALA, which is neurotoxic.

Answer 97

A

CLASS: Muscle Relaxant MECHANISM: Relaxes skeletal muscle by inhibiting excitation-contraction coupling. In combination with agents to manage arrhythmia and renal failure from myoglobinemia. Therapy is highly effective if recognized and treated early. INDICATION: Treat malignant hyperthermia AEs:

Answer 98

A

CLASS: Inhalation Anesthetic MECHANISM: Least soluble volatile agent, highest MAC. Fastest volatile wash-in/wash-out, MAC ~6%, most irritating volatile agent. Least effect on CO among volatiles, may cause bronchoconstriction. INDICATION: AEs: Coughing and laryngospasm with light level anesthesia. Asthmatics exaggerated bronchoconstriction response.

Answer 99

A

CLASS: Barbiturate MECHANISM: Shorter duration of action less cf. thiopental. Suppresses seizures less than thiopental and propofol. INDICATION: Induction or maintenance anesthesia, ECT induction, oral surgery hypnotic (most common) AEs: Greater pain on injection (cf. thiopental), involuntary movements, hiccoughing under anesthesia.

Answer 100

A

CLASS: Inhalation Anesthetic MECHANISM: Newest volatile agent. MAC ~2%, CV effects similar to isoflurane. Low solubility, pleasant odor, lacking airway irritation = indidcated for induction. INDICATION: Induction if inhalation indicated AEs: Significant biotransformation, unclear if metabolites cause and organ toxicity.

Answer 101

A

CLASS: Opioid MECHANISM: Shorter-acting cf. fentanyl, given by bolus injection/infusion, 10x potent cf. fentanyl. INDICATION: Analgesia during anesthesia AEs:

Answer 102

A

CLASS: TCA MECHANISM: Tertiary tricyclic antidepressant, inhibits NE and serotonin reuptake. Central and peripheral anticholinergic effects. No improved mood in "normals" (sedation and difficulty concentrating). Improved mood in a few weeks in depressed patient with tolerance to sedation, but not antidepressant effects. Facilitates falling/staying asleep (usually disturbed in depression) >> less physiologic: increased Stage 4, decreased REM. INDICATION: Depression AEs: Dry mouth, blurred vision, ECG changes (increased resting HR, intracardiac conduction slowing, flat/inverted T wave) = possibly dangerous in those with conduction problems or taking Class I antidysrhythmics. Overdose: fatal malignant arrhythmia (untreated) requires 1-2 weeks supply of pills = easy suicide access in depressed patients. Orthostatic hypotension (a-blockade), lowers seizure threshold (bad in epilepsy), mania (more likely in bipolar disorder), weight gain.

Answer 103

A

CLASS: DNRI MECHANISM: "Wellbutrin" lacks sedative, anticholinergic, orthostatic, and cardiac conduction effects. Believed to act by inhibiting reuptake of NE and dopamine, not serotonin. INDICATION: Depression, nicotine withdrawal ("Zyban" is a controlled release formulation) AEs: Lowers seizure threshold more than any other antidepressant

Answer 104

A

CLASS: Anticonvulsant MECHANISM: In combination with lithium to allow lower dose/toxicity. After first manic episode, continue treatment for 6-12 months until mood stabilization. If manic episodes are separated by severe depression, may need to add antidepressant. If remission lasts many years, may no longer require pharmacotherapy. INDICATION: Bipolar disorder [1st line with lithium] AEs: CYP inducer.

Answer 105

A

CLASS: SSRI MECHANISM: "Celexa" Inhibits reuptake of serotonin. High safety profile: better tolerated than other antidepressants, no sedation, anticholinergic effect, orthostatic hypotension, cardiac conduction issues, weight gain (may aid weight loss), or seizure effect. Lag time 3-4 weeks, before meaningful effect evident (immediate increase in serotonin stimulates presynaptic receptors that initially decreases serotonin synthesis and release, after a few weeks the presynaptic receptors are downregulated) >> long-term increase in serotonin concentration at synapse. Empiric selection, usually start with medium or low (for elderly) dose with follow-up after 1-2 weeks to assess effect >> if AE's acceptable, can increase dose (effects still in lag phase), if no response after some time at high dose or unacceptable AE's >>switch Rx (possibly to different drug class). Hard to gauge efficacy because ~1/3 of major depressive d/o show response to placebo. INDICATION: Depression
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs: Many AE's, but overall incidence and severity is minimal compared to benefit: anxiety, irritability, nausea, decreased libido, anorgasmia, erectile dysfunction. May cause "switch phenomenon" in bipolar disorder (induces manic episode). Serotonin syndrome is potentially fatal (myoclonus, hyperreflexia, confusion, muscle rigidity, tremor, hyperthermia, sweating, tachycardia, coma, seizure): usually due to addition of second drug that inhibits serotonin reuptake or metabolism (e.g. MAO-i + meperidine).
Black Box Warning: increased suicidal ideation in those

Answer 106

A

CLASS: TCA MECHANISM: Secondary tricyclic antidepressant, much less sedation, fewer anticholinergic effects, less weight gain (cf. amitriptyline). INDICATION: Depression AEs: Cardiac conduction effects and lethal overdose (similar to amitriptyline).

Answer 107

A

CLASS: TCA MECHANISM: Tertiary tricyclic antidepressant, inhibits NE and serotonin reuptake. Central and peripheral anticholinergic effects. No improved mood in "normals" (sedation and difficulty concentrating). Improved mood in a few weeks in depressed patient with tolerance to sedation, but not antidepressant effects. Facilitates falling/staying asleep (usually disturbed in depression) >> less physiologic: increased Stage 4, decreased REM. INDICATION: Depression AEs: Dry mouth, blurred vision, ECG changes (increased resting HR, intracardiac conduction slowing, flat/inverted T wave) = possibly dangerous in those with conduction problems or taking Class I antidysrhythmics. Overdose: fatal malignant arrhythmia (untreated) requires 1-2 weeks supply of pills = easy suicide access in depressed patients. Orthostatic hypotension (a-blockade), lowers seizure threshold (bad in epilepsy), mania (more likely in bipolar disorder), weight gain.

Answer 108

A

CLASS: SSRI MECHANISM: "Prozac" Inhibits reuptake of serotonin. High safety profile: better tolerated than other antidepressants, no sedation, anticholinergic effect, orthostatic hypotension, cardiac conduction issues, weight gain (may aid weight loss), or seizure effect. Lag time 3-4 weeks, before meaningful effect evident (immediate increase in serotonin stimulates presynaptic receptors that initially decreases serotonin synthesis and release, after a few weeks the presynaptic receptors are downregulated) >> long-term increase in serotonin concentration at synapse. Empiric selection, usually start with medium or low (for elderly) dose with follow-up after 1-2 weeks to assess effect >> if AE's acceptable, can increase dose (effects still in lag phase), if no response after some time at high dose or unacceptable AE's >>switch Rx (possibly to different drug class). Hard to gauge efficacy because ~1/3 of major depressive d/o show response to placebo. INDICATION: Depression, panic attacks, OCD, only approved SSRi for depression and OCD in children.
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs: Many AE's, but overall incidence and severity is minimal compared to benefit: anxiety, irritability, nausea, decreased libido, anorgasmia, erectile dysfunction. May cause "switch phenomenon" in bipolar disorder (induces manic episode). Serotonin syndrome is potentially fatal (myoclonus, hyperreflexia, confusion, muscle rigidity, tremor, hyperthermia, sweating, tachycardia, coma, seizure): usually due to addition of second drug that inhibits serotonin reuptake or metabolism (e.g. MAO-i + meperidine). CYP inhibition.
Black Box Warning: increased suicidal ideation in those

Answer 109

A

CLASS: TCA MECHANISM: Tertiary tricyclic antidepressant, inhibits NE and serotonin reuptake. Central and peripheral anticholinergic effects. No improved mood in "normals" (sedation and difficulty concentrating). Improved mood in a few weeks in depressed patient with tolerance to sedation, but not antidepressant effects. Facilitates falling/staying asleep (usually disturbed in depression) >> less physiologic: increased Stage 4, decreased REM. INDICATION: Depression AEs: Dry mouth, blurred vision, ECG changes (increased resting HR, intracardiac conduction slowing, flat/inverted T wave) = possibly dangerous in those with conduction problems or taking Class I antidysrhythmics. Overdose: fatal malignant arrhythmia (untreated) requires 1-2 weeks supply of pills = easy suicide access in depressed patients. Orthostatic hypotension (a-blockade), lowers seizure threshold (bad in epilepsy), mania (more likely in bipolar disorder), weight gain.

Answer 110

A

CLASS: MAO-I MECHANISM: Monoamine oxidase inhibitor. Less likely to cause DDI's is selegiline (selective MAO-B brain form inhibitor) >> can use for depression at higher doses than those necessary for Parkinsons. INDICATION: [Second line] reserved for antidepressant non-responders AEs: Many DDI's, potentially fatal (e.g. opioid meperidine has serotonin reuptake inhibition that can lead to serotonin crisis if added to MAO-I). important dietary restriction of tyramine (aged cheese, meat, soy, sauerkraut, beer) >> Tyramine is a sympathomimetic normally metabolized by MAO in the gut, which can cause a hypertensive crisis if enters circulation.

Answer 111

A

CLASS: Alkali Metal MECHANISM: No known physiologic function. Cell membranes poorly able to regulate flux because of low gradient, mood-stabilizing mechanism unclear: increase NE and dopamine release, not serotonin from nerve terminal in response to AP. Slow, complete GI absorption, not protein-bound, distributed in total body water, completely excreted in urine, t1/2 ~1 day. Hyponatremia decreases excretion and prolonged effect in renal failure, wide variability in absorption. Commonly administered as carbonate ion, slow release preps and citrate syrup available (may decrease GI symptoms). INDICATION: Mood stabilization, bipolar disorder and acute mania (neuroleptic + sedative given IM for rapid onset >> several days before stable concentration) AEs: Significant toxicity at 2x therapeutic concentration (mild = nausea, vomiting, diarrhea, abdominal pain, tremor, sedation >> severe = hyperreflexia, cranial nerve and focal neuro signs, nephrogenic diabetes insipidus, seizures, coma, death): must monitor.Thirst, weight gain, drowsiness, T wave flattening.

Answer 112

A

CLASS: a2-agonist MECHANISM: Similar effect to SNRI's, but a2-agonist to increase release of serotonin and NE from nerve terminals (unique mechanism). INDICATION: Depression AEs:

Answer 113

A

CLASS: TCA MECHANISM: Secondary tricyclic antidepressant, much less sedation, fewer anticholinergic effects, less weight gain (cf. amitriptyline). INDICATION: Depression AEs: Cardiac conduction effects and lethal overdose (similar to amitriptyline).

Answer 114

A

CLASS: SSRI MECHANISM: "Paxil" Inhibits reuptake of serotonin. High safety profile: better tolerated than other antidepressants, no sedation, anticholinergic effect, orthostatic hypotension, cardiac conduction issues, weight gain (may aid weight loss), or seizure effect. Lag time 3-4 weeks, before meaningful effect evident (immediate increase in serotonin stimulates presynaptic receptors that initially decreases serotonin synthesis and release, after a few weeks the presynaptic receptors are downregulated) >> long-term increase in serotonin concentration at synapse. Empiric selection, usually start with medium or low (for elderly) dose with follow-up after 1-2 weeks to assess effect >> if AE's acceptable, can increase dose (effects still in lag phase), if no response after some time at high dose or unacceptable AE's >>switch Rx (possibly to different drug class). Hard to gauge efficacy because ~1/3 of major depressive d/o show response to placebo. INDICATION: Depression, panic attacks, OCD
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs: Congenital cardiac malformations if given in first trimester.
Many AE's, but overall incidence and severity is minimal compared to benefit: anxiety, irritability, nausea, decreased libido, anorgasmia, erectile dysfunction. May cause "switch phenomenon" in bipolar disorder (induces manic episode). Serotonin syndrome is potentially fatal (myoclonus, hyperreflexia, confusion, muscle rigidity, tremor, hyperthermia, sweating, tachycardia, coma, seizure): usually due to addition of second drug that inhibits serotonin reuptake or metabolism (e.g. MAO-i + meperidine). CYP inhibition.
Black Box Warning: increased suicidal ideation in those

Answer 115

A

CLASS: MAO-I MECHANISM: Monoamine oxidase inhibitor. Less likely to cause DDI's is selegiline (selective MAO-B brain form inhibitor >> can use for depression at higher doses than those necessary for Parkinsons. INDICATION: [Second line] reserved for antidepressant non-responders AEs: Many DDI's, potentially fatal (e.g. opioid meperidine has serotonin reuptake inhibition that can lead to serotonin crisis if added to MAO-I). important dietary restriction of tyramine (aged cheese, meat, soy, sauerkraut, beer) >> Tyramine is a sympathomimetic normally metabolized by MAO in the gut, which can cause a hypertensive crisis if enters circulation.

Answer 116

A

CLASS: SSRI MECHANISM: "Zoloft" Inhibits reuptake of serotonin. High safety profile: better tolerated than other antidepressants, no sedation, anticholinergic effect, orthostatic hypotension, cardiac conduction issues, weight gain (may aid weight loss), or seizure effect. Lag time 3-4 weeks, before meaningful effect evident (immediate increase in serotonin stimulates presynaptic receptors that initially decreases serotonin synthesis and release, after a few weeks the presynaptic receptors are downregulated) >> long-term increase in serotonin concentration at synapse. Empiric selection, usually start with medium or low (for elderly) dose with follow-up after 1-2 weeks to assess effect >> if AE's acceptable, can increase dose (effects still in lag phase), if no response after some time at high dose or unacceptable AE's >>switch Rx (possibly to different drug class). Hard to gauge efficacy because ~1/3 of major depressive d/o show response to placebo. INDICATION: Depression, panic attacks, OCD, and OCD in children.
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs: Many AE's, but overall incidence and severity is minimal compared to benefit: anxiety, irritability, nausea, decreased libido, anorgasmia, erectile dysfunction. May cause "switch phenomenon" in bipolar disorder (induces manic episode). Serotonin syndrome is potentially fatal (myoclonus, hyperreflexia, confusion, muscle rigidity, tremor, hyperthermia, sweating, tachycardia, coma, seizure): usually due to addition of second drug that inhibits serotonin reuptake or metabolism (e.g. MAO-i + meperidine).
Black Box Warning: increased suicidal ideation in those

Answer 117

A

CLASS: Atypical MECHANISM: Very sedating, but minimal anticholinergic effect or cardiac conduction effect. Weak serotonin/NE reuptake inhibition. Antidepressant action believed to be due to 5-HT2a-antagonism and presynaptic 5-HT1-antagonism (increasing serotonin release). INDICATION: Depression AEs:

Answer 118

A

CLASS: MAO-I MECHANISM: Monoamine oxidase inhibitor. Less likely to cause DDI's is selegiline (selective MAO-B brain form inhibitor >> can use for depression at higher doses than those necessary for Parkinsons. INDICATION: [Second line] reserved for antidepressant non-responders AEs: Many DDI's, potentially fatal (e.g. opioid meperidine has serotonin reuptake inhibition that can lead to serotonin crisis if added to MAO-I). important dietary restriction of tyramine (aged cheese, meat, soy, sauerkraut, beer) >> Tyramine is a sympathomimetic normally metabolized by MAO in the gut, which can cause a hypertensive crisis if enters circulation.

Answer 119

A

CLASS: Anticonvulsant MECHANISM: In combination with lithium to allow lower dose/toxicity. After first manic episode, continue treatment for 6-12 months until mood stabilization. If manic episodes are separated by severe depression, may need to add antidepressant. If remission lasts many years, may no longer require pharmacotherapy. INDICATION: Bipolar disorder [1st line with lithium] AEs: Weight gain, anemia

Answer 120

A

CLASS: TCA MECHANISM: Tertiary tricyclic antidepressant, inhibits NE and serotonin reuptake. Central and peripheral anticholinergic effects. No improved mood in "normals" (sedation and difficulty concentrating). Improved mood in a few weeks in depressed patient with tolerance to sedation, but not antidepressant effects. Facilitates falling/staying asleep (usually disturbed in depression) >> less physiologic: increased Stage 4, decreased REM. INDICATION: Depression AEs: Dry mouth, blurred vision, ECG changes (increased resting HR, intracardiac conduction slowing, flat/inverted T wave) = possibly dangerous in those with conduction problems or taking Class I antidysrhythmics. Overdose: fatal malignant arrhythmia (untreated) requires 1-2 weeks supply of pills = easy suicide access in depressed patients. Orthostatic hypotension (a-blockade), lowers seizure threshold (bad in epilepsy), mania (more likely in bipolar disorder), weight gain.

Answer 121

A

CLASS: SNRI MECHANISM: "Cymbalta" Serotonin and NE reuptake inhibitor. May be effective in SSRI non-responders. Very safe, but cause sedation. INDICATION: Depression
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs:

Answer 122

A

CLASS: SSRI MECHANISM: "Lexapro" Active isomer of citalopram. Inhibits reuptake of serotonin. High safety profile: better tolerated than other antidepressants, no sedation, anticholinergic effect, orthostatic hypotension, cardiac conduction issues, weight gain (may aid weight loss), or seizure effect. Lag time 3-4 weeks, before meaningful effect evident (immediate increase in serotonin stimulates presynaptic receptors that initially decreases serotonin synthesis and release, after a few weeks the presynaptic receptors are downregulated) >> long-term increase in serotonin concentration at synapse. Empiric selection, usually start with medium or low (for elderly) dose with follow-up after 1-2 weeks to assess effect >> if AE's acceptable, can increase dose (effects still in lag phase), if no response after some time at high dose or unacceptable AE's >>switch Rx (possibly to different drug class). Hard to gauge efficacy because ~1/3 of major depressive d/o show response to placebo. INDICATION: Depression
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs: Many AE's, but overall incidence and severity is minimal compared to benefit: anxiety, irritability, nausea, decreased libido, anorgasmia, erectile dysfunction. May cause "switch phenomenon" in bipolar disorder (induces manic episode). Serotonin syndrome is potentially fatal (myoclonus, hyperreflexia, confusion, muscle rigidity, tremor, hyperthermia, sweating, tachycardia, coma, seizure): usually due to addition of second drug that inhibits serotonin reuptake or metabolism (e.g. MAO-i + meperidine).
Black Box Warning: increased suicidal ideation in those

Answer 123

A

CLASS: SSRI MECHANISM: "Luvox" Inhibits reuptake of serotonin. High safety profile: better tolerated than other antidepressants, no sedation, anticholinergic effect, orthostatic hypotension, cardiac conduction issues, weight gain (may aid weight loss), or seizure effect. Lag time 3-4 weeks, before meaningful effect evident (immediate increase in serotonin stimulates presynaptic receptors that initially decreases serotonin synthesis and release, after a few weeks the presynaptic receptors are downregulated) >> long-term increase in serotonin concentration at synapse. Empiric selection, usually start with medium or low (for elderly) dose with follow-up after 1-2 weeks to assess effect >> if AE's acceptable, can increase dose (effects still in lag phase), if no response after some time at high dose or unacceptable AE's >>switch Rx (possibly to different drug class). Hard to gauge efficacy because ~1/3 of major depressive d/o show response to placebo. INDICATION: Depression
SSRI (generally) broad range of uses: OCD, panic disorders, PTSD, PMDD, social anxiety disorder, bulemia AEs: Many AE's, but overall incidence and severity is minimal compared to benefit: anxiety, irritability, nausea, decreased libido, anorgasmia, erectile dysfunction. May cause "switch phenomenon" in bipolar disorder (induces manic episode). Serotonin syndrome is potentially fatal (myoclonus, hyperreflexia, confusion, muscle rigidity, tremor, hyperthermia, sweating, tachycardia, coma, seizure): usually due to addition of second drug that inhibits serotonin reuptake or metabolism (e.g. MAO-i + meperidine). CYP inhibition.
Black Box Warning: increased suicidal ideation in those

Answer 124

A

CLASS: Anticonvulsant MECHANISM: In combination with lithium to allow lower dose/toxicity. After first manic episode, continue treatment for 6-12 months until mood stabilization. If manic episodes are separated by severe depression, may need to add antidepressant. If remission lasts many years, may no longer require pharmacotherapy. INDICATION: Bipolar disorder [1st line with lithium], not mania AEs:

Answer 125

A

CLASS: Atypical MECHANISM: Very sedating, but minimal anticholinergic effect or cardiac conduction effect. Weak serotonin/NE reuptake inhibition. Antidepressant action believed to be due to 5-HT2a-antagonism and presynaptic 5-HT1-antagonism (increasing serotonin release). INDICATION: Depression AEs:

Answer 126

A

CLASS: SNRI MECHANISM: "Effexor" Serotonin and NE reuptake inhibitor. May be effective in SSRI non-responders. Very safe, but cause sedation. INDICATION: Depression AEs:

Answer 127

A

CLASS: MECHANISM: Anticholinergic INDICATION: Treat early extrapyramidal effects (akathisia, dystonia, rigidity) AEs:

Answer 128

A

<p class="large" style="text-align: center;">CLASS: Phenothiazine MECHANISM: Antipsychotic, "neuroleptic," orally effective (as are all antipsychotics listed) and IM (like haloperidol, ziprasidone, olanzapine), rarely given IV (because of profound vasodilatory effect).  Very dirty drug, competitive antagonist at: dopamine D2 (primary antipsychotic effect, prefrontal and limbic cortices), muscarinic Ach (much of AE's: dry mouth, sedation), histamine H1, a-adrenergic (AE's: orthostatic hypotension), 5-HT2 receptors. In normals: diminishes all behavior and less/slower response to stimuli.  High dose >> catatonic state with preserved consciousness and memory (can later describe dysphoric sensation).  In psychotics: improvement in thought disorder (schizophrenics lose delusions/hallucinations, more ordered thinking, remaining hallucinations more easily recognized as unreal).  Antiemesis (blocks DA receptors in chemoreceptor trigger zone).  Tolerance does not develop to this or any antipsychotics. INDICATION: Antipsychotic, schizophrenia AEs: Sedation, blurred vision, urinary retention & dry mouth (anticholinergic effects), orthostatic hypotension & nasal stuffiness (a-blockade), lowers seizure threshold (cautious use in epileptics), increased prolactin secretion (DA-block).  Jaundice (bile stasis)
Extrapyramidal effects (DA-block in basal ganglia) = akathisia (uncomfortable inability to sit still and appear agitated), dystonia (uncomfortable/embarrassing contractions of the face and neck), rigidity (indistinguishable from Parkinson's) are three effects that appear early and are dose-dependent (readily treated by anticholinergics: trihexyphenidyl, benztropine; or by H1-antagonist: diphenhydramine). Tardive dyskinesia occurs after prolonged therapy (involuntary, repetitive, stereotyped movements of the face believed to result from denervation supersensitivity at dopamine receptors, e.g. lip smacking, blinking, grimacing, tongue protruding) >> suppressed by increased dose (may be permanent in 50%).
Neuroleptic malignant syndrome = rare, hyperthermia (from muscle contraction), stupor, myoglobinemia, elevated CK.  Resembles malignant hyperthermia (reaction to anesthetics).</p>

Answer 129

A

CLASS: Atypical MECHANISM: Most effective antipsychotic (but, most toxic), orally effective. Less/no activity at DA & ACh receptors = extrapyramidal effects very rare (cf. chlorpromazine), 5-HT2-blocker (responsible for antipsychotic action), potent a-antagonist. INDICATION: Antipsychotic AEs: Orthostatic hypotension (a-block, common), weight gain, diabetes, seizure, agranulocytosis (regular monitoring WBC). More expensive cf. older drugs.

Answer 130

A

CLASS: Antihistamine MECHANISM: Histamine H1 antagonist INDICATION: Treat early extrapyramidal effects (akathisia, dystonia, rigidity) AEs:

Answer 131

A

CLASS: Antiemetic MECHANISM: Antiemetic (like all "classical" antipsychotics), pharmacologically similar to haloperidol, but only marketed as antiemetic because nauseated, non-psychotic patients don't appreciate being prescribed an antipsychotic. Excellent antiemetic effects achieved at doses below those causing sedation or dysphoria (in normals). Less orthostatic hypotension cf. prochlorperazine. IV and IM only. INDICATION: Antiemesis AEs: Rare extrapyramidal effects.

Answer 132

A

CLASS: Phenothiazine MECHANISM: Antipsychotic with less anticholinergic effect = less sedation, fewer hypotensive effects cf. chlorpromazine, orally effective. Fatty acid ester dissolved in oil (like haloperidol) available for long-lasting deep IM injection. INDICATION: Long-term tx of orally non-compliant patient (deep IM injection, like haloperidol) AEs: More extrapyramidal reactions (more potent D2-antagonists) cf. chlorpromazine.

Answer 133

A

CLASS: Butyrophenone MECHANISM: Very common antipsychotic, little M-antagonist or a-antagonist activity (cf. chlorpromazine) = little sedation or hypotension, orally effective, IV, and IM. Fatty acid ester dissolved in oil (like fluphenazine) available for long-lasting deep IM injection. INDICATION: Acute psychosis (IV or IM), in those without psychosis diagnosis, e.g. ICU-associated psychosis, and for long-term tx of orally non-compliant patient (deep IM injection, like fluphenazine) AEs: High incidence of extrapyramidal effects.

Answer 134

A

CLASS: Atypical MECHANISM: Second most effective antipsychotic (better than phenothiazines and butyrophenones), orally effective, IM (like haloperidol, ziprasidone, chlorpromazine). Less/no activity at DA & ACh receptors = extrapyramidal effects very rare (cf. chlorpromazine), 5-HT2-blocker (responsible for antipsychotic action), potent a-antagonist. No seizures or agranulocytosis (cf. clozapine, though very closely related structure) INDICATION: Antipsychotic AEs: Orthostatic hypotension (a-block, common), weight gain, diabetes. More expensive cf. older drugs.

Answer 135

A

CLASS: Antiemetic MECHANISM: Antiemetic (like all "classical" antipsychotics), pharmacologically similar to chlorpromazine, but only marketed as antiemetic because nauseated, non-psychotic patients don't appreciate being prescribed an antipsychotic. Many preparations available: tablet, liquid, suppository, injection. INDICATION: Antiemesis AEs: More orthostatic hypotension cf. droperidol

Answer 136

A

CLASS: Atypical MECHANISM: Second most effective antipsychotic (better than phenothiazines and butyrophenones), orally effective. Available as long-lasting microsphere deep IM injection embedded in polymer (cf. haloperidol & fluphenazine). Less/no activity at DA & ACh receptors = extrapyramidal effects very rare (cf. chlorpromazine), 5-HT2-blocker (responsible for antipsychotic action), potent a-antagonist. INDICATION: Long-term tx of orally non-compliant patient (deep IM injection, cf. haloperidol & fluphenazine) AEs: Orthostatic hypotension (a-block, common), extrapyramidal effects (high dose), weight gain. More expensive cf. older drugs.

Answer 137

A

CLASS: Phenothiazine MECHANISM: Antipsychotic with greater anticholinergic effect = fewer extrapyramidal effects cf. chlorpromazine, orally effective. INDICATION: Antipsychotic AEs: More sedation (anticholinergic) & hypotensive effects (a-block) cf. chlorpromazine.

Answer 138

A

CLASS: MECHANISM: Anticholinergic INDICATION: Treat early extrapyramidal effects (akathisia, dystonia, rigidity) AEs:

Answer 139

A

CLASS: Atypical MECHANISM: Same efficacy as older antipsychotics (phenothiazines and butyrophenones), orally effective. Less/no activity at DA & ACh receptors = extrapyramidal effects very rare (cf. chlorpromazine), 5-HT2-blocker (responsible for antipsychotic action), potent a-antagonist. No weight gain (cf. clozapine, olanzapine, risperidone). INDICATION: Antipsychotic AEs: Orthostatic hypotension (a-block, common). More expensive cf. older drugs.

Answer 140

A

CLASS: Atypical MECHANISM: Same efficacy as older antipsychotics (phenothiazines and butyrophenones), orally effective. Less/no activity at DA & ACh receptors = extrapyramidal effects very rare (cf. chlorpromazine), 5-HT2-blocker (responsible for antipsychotic action), potent a-antagonist. No weight gain (cf. clozapine, olanzapine, risperidone). INDICATION: Antipsychotic AEs: Orthostatic hypotension (a-block, common). More expensive cf. older drugs.

Answer 141

A

CLASS: Phenothiazine MECHANISM: Antipsychotic with less anticholinergic effect = less sedation, fewer hypotensive effects cf. chlorpromazine, orally effective. INDICATION: Antipsychotic AEs: More extrapyramidal reactions (more potent D2-antagonists) cf. chlorpromazine, may cause cardiac QT prolongation.

Answer 142

A

CLASS: Atypical MECHANISM: Same efficacy as older antipsychotics (phenothiazines and butyrophenones), orally effective, IM (like haloperidol, chlorpromazine, olanzapine). Unique atypical antipsychotic, partial agonist at dopamine D2 and 5-HT1A receptors. No weight gain (cf. clozapine, olanzapine, risperidone). INDICATION: Antipsychotic AEs: Orthostatic hypotension (a-block, common), extrapyramidal effects & QT prolongation (rare, may predispose dysrhythmia). More expensive cf. older drugs.

Brainscape's Knowledge GenomeTM

Brain Track 3 Drugs Flashcards

Brainscape's Knowledge Genome^TM